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. 2013 Oct 31;306(1):G48–G58. doi: 10.1152/ajpgi.00234.2013

Fig. 7.

Fig. 7.

FXR and small interfering KRAS (siKRAS) expression in human colon cancer cell lines and the predicted role of FXR in colon cancer development. A: relative mRNA levels of FXR in colon cancer cell lines treated with siKRAS. B: relative mRNA levels of KRAS in colon cancer cell lines confirming knockdown of KRAS. Data are expressed as means + SE. *P < 0.05 compared with nontargeting (NT) siRNA controls. Hyper-Me, hypermethylation. C: colon cancer is initiated by an acquired mutation within genes involved in WNT signaling (APC or β-catenin) or DNA repair signaling. Promotion to an adenoma often occurs through CpG island hypermethylation and acquired KRAS mutations (22). Our results indicate that FXR is also silenced during this early period of adenoma formation and correlates with EMT and oncogenic signaling of PI3K, suggesting that FXR silencing contributes to colon cancer progression and/or metastasis. If FXR expression is restored by inhibition of DNA methylation or KRAS signaling and activated by synthetic FXR ligands, this may help restore normal cancer cell phenotype, slow cancer progression, and/or sensitize cancer cells to chemotherapy.